title: "Week 1: Resuscitation"

Week 1: Resuscitation

1. The ABCDE Approach & Deteriorating Patient

The DETECT System

The DETECT approach provides a systematic method for assessing deteriorating patients:

LetterAssessment
DDanger (personal safety first)
EEnd of bed assessment
TTalk to the patient
EExamine systematically
CCall for help
TTreatment/Transfer

ABCDE Assessment

Systematic approach to the deteriorating patient

Deteriorating Patient: ABCDE

ABCDE approach: treat life-threatening problems as you find them — do not complete the full assessment before intervening. If the airway is compromised, secure it before moving

ABCDEFG Systematic Assessment

SystemLook/Listen/FeelKey Observations
A - AirwayStridor, gurgling, snoringPatent? Obstructed? Partial?
B - BreathingRR (Respiratory Rate), SpO2 (Peripheral Oxygen Saturation), chest movement, breath soundsTachypnoea? Hypoxia? Work of breathing?
C - CirculationHR (Heart Rate), BP (Blood Pressure), CRT (Capillary Refill Time), colour, urine outputTachycardia? Hypotension? Cool peripheries?
D - DisabilityGCS (Glasgow Coma Scale), pupils, BSL (Blood Sugar Level)Altered consciousness? Hypoglycaemia?
E - ExposureTemperature, rashes, woundsFever? Hypothermia? Source?
F - FluidsFluid balance, oedemaHypovolaemia? Overload?
G - GlucoseBSLUnder 4 or over 11 mmol/L?

AVPU - Rapid Consciousness Assessment

AVPU Scale
  • A - Alert: eyes open spontaneously, oriented
  • V - Voice: responds to verbal commands, may be confused
  • P - Pain: responds only to painful stimulus
  • U - Unresponsive: no response to any stimulus

AVPU vs GCS: AVPU is a quick screening tool. If the patient is not Alert, calculate full GCS.

  • A ≈ GCS 15
  • V ≈ GCS 13
  • P ≈ GCS 8
  • U ≈ GCS 3
SBAeasyAVPUconsciousness-assessmentprimary-survey
AVPU stands for?
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The 7 E's - Patients at Risk of Deterioration

Emergency presentations: Haven't been fully assessed yet; undifferentiated illness can rapidly declare itself as something serious.

Elderly patients: Reduced physiological reserve (cardiac output, respiratory function, renal clearance). They compensate poorly and decompensate suddenly. Atypical presentations mask severity (afebrile sepsis, painless MI).

Existing comorbidities: Each comorbidity reduces reserve. A patient with COPD, CCF, and CKD has no margin for error when stressed.

Extreme illness severity: Already at the edge of compensation. Any further insult tips them over.

Emerging from anaesthesia: Residual anaesthetic effects (respiratory depression, hypotension), incomplete reversal of NMBAs, pain causing hypertension/tachycardia, risk of laryngospasm.

Exsanguinating patients: Obvious - haemodynamic instability, coagulopathy (especially trauma triad: hypothermia, acidosis, coagulopathy).

Exiting critical care units: Were sick enough to need ICU. Often deconditioned, may have unrecognised complications, and ward monitoring is less intensive. The transition period is high-risk.

  • Emergency presentations (undifferentiated illness)
  • Elderly patients (reduced reserve, atypical signs)
  • Existing comorbidities (less physiological reserve)
  • Extreme illness severity (near decompensation)
  • Emerging from anaesthesia (residual drug effects)
  • Exsanguinating patients (major haemorrhage)
  • Exiting critical care units (step-down risk)
Clinical Pearl

These patients need closer monitoring and lower thresholds for escalation.

ISBAR Handover Framework

LetterComponentExample
IIntroduction"I'm Ian, the medical student looking after..."
SSituation"I'm calling about Mrs Smith who has become hypotensive"
BBackground"She's day 2 post-op cholecystectomy, PMHx of HTN, DM"
AAssessment"BP 85/50, HR 110, looks pale, I think she may be bleeding"
RRecommendation"I think she needs urgent review and consideration for return to theatre"

ISBAR Handover

Structured clinical communication framework


2. Basic Life Support (BLS)

The DRSABCD Algorithm

StepActionDetails
DDangerCheck for hazards (syringes, electricity, spills)
RResponseShout "Are you okay?" + shoulder squeeze
SSend for helpPress emergency button, call 000/MET call
AAirwayHead tilt, chin lift (unless C-spine)
BBreathingLook, listen, feel for 10 seconds
CCPRIf not breathing normally, start compressions
DDefibrillationAttach AED/pads as soon as available

DRSABCD (Basic Life Support)

First 60 seconds of cardiac arrest response

CPR: The Critical Numbers

ParameterTargetEvidence
Compression depth5 cm (at least 1/3 chest depth)Stiell et al., 2014
Compression rate100-120/minARC Guidelines
Compression:ventilation ratio30:2ARC Guidelines
Swap compressorsEvery 2 minutesPrevents fatigue
Chest recoilCompleteAllow full recoil between compressions

Each minute without defibrillation reduces survival by 10% - this is why minimising interruptions to CPR is critical.

During cardiac arrest, the heart can't generate its own perfusion. CPR creates artificial circulation by compressing the heart between the sternum and spine.

Compression phase: Blood is ejected from the heart Recoil phase: Heart refills with blood

If you don't allow full recoil, the heart can't refill properly - subsequent compressions become ineffective. This is why leaning on the chest between compressions is harmful.

Coronary perfusion pressure (CPP) is what determines whether the heart can be restarted. It takes 10-15 compressions to build up adequate CPP. Each pause (for rhythm check, airway, etc.) resets this - which is why minimising interruptions is critical.

Airway Management

  • Head tilt chin lift: Primary technique (avoid if C-spine suspected)
  • Jaw thrust: Use if C-spine injury possible
  • Intubation NOT shown to improve outcomes in cardiac arrest
  • Bag valve mask or LMA (Laryngeal Mask Airway) adequate in first instance
Warning

Warning: Avoid over-ventilation! Increases thoracic pressure, decreases venous return, and reduces chance of ROSC.

During CPR, the only blood flow comes from chest compressions. This already provides marginal perfusion.

The problem with bagging too fast/hard:

  1. Increased intrathoracic pressure - each breath raises pressure inside the chest
  2. Impaired venous return - the vena cava gets compressed; blood can't get back to the heart
  3. Reduced cardiac output - less preload = less to pump out during compressions
  4. Gastric insufflation - air enters stomach → aspiration risk + diaphragm splinting

Landmark study: Aufderheide et al. showed that hyperventilation during CPR decreased coronary perfusion pressure and survival rates in animal models.

Target ventilation rate:

  • Unprotected airway: 30:2 (pause compressions for 2 breaths)
  • Advanced airway: 10 breaths/min (1 every 6 seconds), asynchronous with compressions

Clinical tip: The person bagging often gets caught up in the chaos and bags too frequently. Assign someone to count and call out ventilations.

Two-Hand Bag Valve Mask Technique

  • Use C and E grip on mandible
  • Provide jaw thrust
  • Leave pillow behind head
  • Second person squeezes bag

3. Advanced Life Support (ALS)

Shockable vs Non-Shockable Rhythms

ShockableNon-Shockable
Ventricular Fibrillation (VF (Ventricular Fibrillation))Asystole
Pulseless Ventricular Tachycardia (pVT (Ventricular Tachycardia))Pulseless Electrical Activity (PEA (Pulseless Electrical Activity))

How to Identify:

  • VF (Ventricular Fibrillation)/pVT (Ventricular Tachycardia): "Wide and fast" or "wide and weird"
  • Asystole: Flat line - terrible prognosis
  • PEA (Pulseless Electrical Activity): Organised rhythm but NO pulse - think profound hypotension

The COACHED Defibrillation Script

COACHED
LetterAction
CContinue compressions
OOxygen away (from chest)
AAll else clear
CCharging
HHands off - check rhythm
EEvaluate rhythm (shock or no shock)
DDefibrillate (if shockable) then immediately resume CPR

Drug Timing in ALS

DrugDoseTiming
Adrenaline (Shockable)1 mg IVAfter 2nd shock, then every 2nd loop (4 min)
Adrenaline (Non-Shockable)1 mg IVImmediately, then every 2nd loop (4 min)
Amiodarone300 mg IVAfter 3rd shock (shockable rhythms only)
Amiodarone (repeat)150 mg IVAfter 5th shock if refractory VF

In shockable rhythms, give adrenaline 1 mg IV after the 2nd shock, then every 4 minutes (every second loop).

In non-shockable rhythms, give adrenaline 1 mg IV immediately, then every 4 minutes.

Give amiodarone 300 mg IV after the 3rd shock, then 150 mg IV after the 5th shock if refractory VF/pVT.

Reversible Causes: 4 H's and 4 T's

4 H's and 4 T's
4 H'sManagement4 T'sManagement
HypoxiaVentilate with 100% O2Tension PneumothoraxNeedle decompression
HypovolaemiaIV fluids, blood productsTamponade (cardiac)Pericardiocentesis
Hyper/hypokalaemiaCheck VBG, correct K+Thrombosis (PE/MI)Thrombolysis/PCI
HypothermiaActive warmingToxinsSpecific antidotes

PEA (Pulseless Electrical Activity) - Think Causes of Profound Hypotension

  • Septic shock
  • Massive MI (Myocardial Infarction)
  • Bleeding/trauma
  • Poisoning
  • Obstruction: Tension Pneumothorax, tamponade, massive PE (Pulmonary Embolism)
Clinical Pearl

Traumatic PEA requires volume resuscitation, not standard ALS

The heart is often structurally fine but has nothing to pump. Standard ACLS fails because adrenaline vasoconstricts an empty tank. Save these patients with massive transfusion, bleeding control, and relieving obstructions (tamponade, tension pneumothorax).

Advanced Life Support Algorithm

Practice the ALS algorithm with real-time drug timing, 2-minute CPR cycles, and training scenarios.


4. Pharmacology in Critical Care

High Risk Medications: A PINCH

A PINCH

These medications have narrow therapeutic windows or severe consequences when errors occur:

Anti-infectives (A): Aminoglycosides (gentamicin) and vancomycin have concentration-dependent toxicity. Too much → permanent hearing loss, kidney failure. Too little → treatment failure. Requires therapeutic drug monitoring (trough levels).

Potassium/Electrolytes (P): IV potassium chloride given too fast causes fatal arrhythmia. Concentrated KCl should never be on a ward - it's been involved in multiple accidental deaths. Hypertonic saline can cause central pontine myelinolysis.

Insulin (I): Hypoglycaemia can be fatal or cause permanent brain damage. Common errors: wrong formulation (rapid vs long-acting), wrong units, sliding scale confusion. Always independent double-check insulin doses.

Narcotics/Sedatives (N): Respiratory depression, especially in opioid-naïve patients, elderly, renal impairment, or with other CNS depressants. Can be insidious - patient looks comfortable until they stop breathing.

Chemotherapy (C): Extremely toxic with complex dosing schedules. Errors can be fatal (vincristine intrathecal = death). Usually requires specialised pharmacist verification and dedicated administration protocols.

Heparin/Anticoagulants (H): Bleeding risk, especially with impaired renal function (enoxaparin), drug interactions (warfarin), or when bridging between agents. aPTT/INR monitoring critical.

LetterCategoryExamplesKey Concerns
AAnti-infectivesGentamicin, VancomycinOtotoxicity, Nephrotoxicity
PPotassium/ElectrolytesKCl, NaCl, MgSO4Cardiac arrest if wrong dose
IInsulinAll formulationsHypoglycaemia, variable absorption
NNarcotics/SedativesMorphine, Fentanyl, MidazolamRespiratory depression
CChemotherapyVariousNarrow therapeutic window
HHeparin/AnticoagulantsUFH, Enoxaparin, WarfarinBleeding

Pharmacokinetic Changes in Critical Illness

PhaseChangeClinical Implication
AbsorptionDelayed/impaired GI absorptionUnpredictable oral drug levels, consider IV (Intravenous)
DistributionIncreased Vd (fluid overload), decreased protein bindingIncreased free drug, may need dose adjustment
MetabolismDecreased hepatic clearance (sepsis, hypothermia)Prolonged drug effects
EliminationDecreased renal clearance (AKI (Acute Kidney Injury))Accumulation, dose reduce renally-cleared drugs

Patients at Highest Risk

  • Renal impairment (AKI (Acute Kidney Injury)/CKD (Chronic Kidney Disease))
  • Hepatic impairment
  • Elderly
  • Obese
  • Neonates/children
  • Multiple sedating medications
  • Substance misuse history

5. Intubation Pharmacology

Induction Agents

DrugDoseOnsetDurationKey Features
Propofol1.5-2.5 mg/kg15-45 sec5-10 minHypotension, pain on injection
Ketamine1-2 mg/kg30-60 sec10-20 minMaintains BP (Blood Pressure), bronchodilator, emergence phenomena
Thiopentone3-5 mg/kg15-30 sec5-10 minHypotension, decreases ICP (Intracranial Pressure)
Midazolam0.1-0.3 mg/kg1-2 min15-30 minAmnestic, respiratory depression

Ketamine is preferred in [] patients (maintains BP (Blood Pressure)) and [] (bronchodilator).

Ketamine maintains BP (Blood Pressure) by causing sympathetic stimulation via inhibiting catecholamine reuptake, which releases endogenous adrenaline and noradrenaline.

Caution: In catecholamine-depleted patients (maxed-out vasopressors), this mechanism fails → ketamine can cause hypotension.

Ketamine is ideal for asthmatic patients requiring intubation — it causes bronchodilation via direct smooth muscle relaxation and β2-agonist effect from catecholamine release.

Clinical Pearl

Ketamine maintains BP via sympathetic stimulation (catecholamine reuptake inhibition).

Haemodynamic stability mechanism:

  • Inhibits catecholamine reuptake → releases endogenous adrenaline/noradrenaline
  • Increases HR (Heart Rate), SVR (Systemic Vascular Resistance), and BP (Blood Pressure)
  • Sympathetic effect counteracts ketamine's direct myocardial depression
  • Net result: preserved or increased BP (Blood Pressure)

Bronchodilation mechanism:

  • Direct smooth muscle relaxation
  • Inhibition of vagal pathways (anticholinergic-like)
  • Catecholamine release (β2-agonist effect)

Trade-off: Emergence phenomena (vivid dreams, dissociation) in ~10-20% - mitigated by co-administration of benzodiazepines.

Neuromuscular Blocking Agents

DrugTypeDoseOnsetDurationKey Points
SuxamethoniumDepolarising1-1.5 mg/kg30-60 sec5-10 minFASTEST onset, contraindicated in hyperkalaemia, burns, denervation
RocuroniumNon-depolarising0.6-1.2 mg/kg60-90 sec30-60 minCan be reversed with Sugammadex
VecuroniumNon-depolarising0.1 mg/kg2-3 min30-40 minMinimal cardiovascular effects
Warning

Suxamethonium Contraindications:

Suxamethonium is a depolarising NMBA - it mimics acetylcholine and causes sustained muscle depolarisation. This triggers K+ efflux from muscle cells.

Normal patients: ~0.5 mmol/L K+ rise (clinically insignificant)

Dangerous conditions cause massive K+ release:

  • Burns/denervation/immobility >24h: After ~24 hours, extrajunctional ACh receptors upregulate across the entire muscle membrane (not just the motor endplate). Suxamethonium depolarises all of these → massive K+ efflux → cardiac arrest
  • Existing hyperkalaemia: Even a small additional K+ rise tips into arrhythmia territory
  • Myopathies: Abnormal muscle membranes → unpredictable K+ release

Malignant hyperthermia is a separate mechanism - suxamethonium triggers uncontrolled Ca2+ release from sarcoplasmic reticulum → sustained muscle contraction → hyperthermia, rhabdomyolysis, death.

Safe alternative: Rocuronium (can be rapidly reversed with sugammadex if needed)

  • Hyperkalaemia or risk factors for hyperkalaemia
  • Burns over 24 hours old
  • Denervation injuries
  • MH susceptibility
  • Myopathies

Reversal Agents

Sugammadex - A modified cyclodextrin that forms a tight 1:1 complex around rocuronium/vecuronium molecules, physically "encapsulating" them. The NMBA becomes trapped and inactive. This is dose-dependent and complete - you can reverse even profound blockade rapidly (within 2-3 minutes at high doses). It's specific to aminosteroid NMBAs only.

Neostigmine - An acetylcholinesterase inhibitor. It increases ACh at the neuromuscular junction by preventing breakdown. More ACh competes with the NMBA for binding sites. Limitations:

  • Can only reverse partial blockade (needs some recovery already)
  • Increases ACh everywhere (including heart → bradycardia, gut → secretions)
  • Must give with glycopyrrolate or atropine to block muscarinic effects
  • Cannot reverse deep blockade

Flumazenil - Competitive antagonist at GABA-A receptors. Caution: Can precipitate seizures in benzodiazepine-dependent patients or those on seizure prophylaxis. Short half-life (1 hour) vs long-acting benzos → may need redosing.

Naloxone - Competitive opioid receptor antagonist. Caution: Can precipitate acute withdrawal and severe pain. Start with low doses (0.04-0.1 mg) and titrate to respiratory rate, not consciousness. Short half-life (30-90 min) vs long-acting opioids → watch for renarcotisation.

Sugammadex (2-16 mg/kg) reverses rocuronium/vecuronium by encapsulation (rapid, complete reversal).

Neostigmine (0.05 mg/kg + glycopyrrolate) is an acetylcholinesterase inhibitor; only reverses partial blockade.

Flumazenil (0.2-1 mg) reverses benzodiazepines but can precipitate seizures in dependent patients.

Naloxone (0.4-2 mg) reverses opioids; short half-life → watch for renarcotisation.

AgentReversesDoseMechanism
SugammadexRocuronium, Vecuronium2-16 mg/kgEncapsulates aminosteroid NMBAs
NeostigmineNon-depolarising NMBAs0.05 mg/kg (+ glycopyrrolate)Acetylcholinesterase inhibitor
FlumazenilBenzodiazepines0.2-1 mgCompetitive GABA antagonist
NaloxoneOpioids0.4-2 mgCompetitive opioid antagonist

6. Practice Questions

SBAeasyBLSDRSABCD
67y|M
GCS
unresponsive
Syncope

What is your NEXT action?

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SBAmediumALSVF
During a cardiac arrest, the monitor shows irregular, chaotic electrical activity with no discernible P waves or QRS (QRS Complex) complexes. What is the most appropriate next step?
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SBAmediumALSPEA
A patient is in cardiac arrest with PEA (Pulseless Electrical Activity). You are now on your 4th cycle of CPR (Cardiopulmonary Resuscitation). When should adrenaline be given in non-shockable rhythms?
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SBAeasyCPRBLS
What is the recommended depth of chest compressions during adult CPR (Cardiopulmonary Resuscitation)?
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SBAmediumintubationpharmacology
45y|F
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SBAmediumintubationNMBAs
48y
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SBAeasypharmacologyA PINCH
The category NOT included in the 'A PINCH' high-risk medication mnemonic is:
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SBAeasyALSdefibrillation
During the COACHED defibrillation sequence, what does the 'O' stand for?
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SBAmediumpharmacologyaminoglycosides
A septic patient in ICU (Intensive Care Unit) is receiving gentamicin. Which monitoring is ESSENTIAL?
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SBAeasyDETECTdeteriorating patient
In the DETECT approach to the deteriorating patient, what does the first 'E' stand for?
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SBAmedium4Hs4Tstamponade
A patient in cardiac arrest has PEA (Pulseless Electrical Activity) with a rate of 40/min. Ultrasound shows a large pericardial effusion with right ventricular collapse. What is the most likely reversible cause?
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SBAmediumreversal agentssugammadex
Which agent can rapidly reverse rocuronium-induced neuromuscular blockade?
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SBAeasyairwayOPA
How do you correctly size an oropharyngeal airway (OPA)?
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SBAeasyrhythm recognitionasystole
You are performing CPR (Cardiopulmonary Resuscitation). The monitor shows a completely flat line with no electrical activity. What is this rhythm?
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SBAhardBLSCPR
During CPR (Cardiopulmonary Resuscitation), an advanced airway is in place (ETT (Endotracheal Tube)/SGA) and you have capnography. Which ventilation strategy is recommended?
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SBAhardRSIIntubation
During rapid sequence intubation you obtain a Cormack–Lehane grade 3 view (only epiglottis visible). What is the BEST immediate adjunct to improve first-pass success?
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7. ECG (Electrocardiogram) Interpretation

ECG (Electrocardiogram) Technical Basics

Normal 12-lead ECG (example)LITFL ECG Library (CC BY-NC-SA 4.0)

At standard paper speed of 25mm/s, a big square is 0.2 seconds and a small square is 0.04 seconds

Standard calibration: 10 mm vertical equals 1 mV

Heart rate calculation: Rate = 300 divided by the number of big boxes between each QRS complex

Alternative rate method: 1500 divided by the number of small boxes between QRS complexes

Rate ladder: 300-150-100-75-60-50 for 1-2-3-4-5-6 big boxes between QRS complexes

For irregular rhythms, count the QRS complexes in 6 seconds (30 big boxes) and multiply by 10

ECG axis: Lead I positive + aVF positive = Normal axis (-30° to +90°). The electrical vector points left and inferiorly — this is the most common finding.

ECG axis: Lead I positive + aVF negative = Left axis deviation (more negative than -30°). Think left anterior fascicular block, inferior MI, or LVH.

ECG axis: Lead I negative + aVF positive = Right axis deviation (more positive than +90°). Think RVH, PE, lateral MI, or left posterior fascicular block.

ECG axis: Lead I negative + aVF negative = Extreme axis deviation ("no man's land"). Think ventricular rhythm, severe RVH, or lead misplacement.

Normal QRS axis is -30 to +90 degrees

Left axis deviation is more negative than -30 degrees

Right axis deviation is more positive than +90 degrees

6-Step Approach to Rhythm Strips

6 Questions for Rhythm Strip Analysis
  1. Is there any electrical activity present?
  2. What is the ventricular (QRS) rate?
  3. Is the QRS rhythm regular or irregular?
  4. Is the QRS width normal or broad?
  5. Is atrial activity (P waves) present?
  6. How is atrial activity related to ventricular activity?

Rapid Tachycardia Triage (Narrow vs Wide)

Regular narrow-complex tachycardia is usually SVT or atrial flutter with fixed block

Irregular narrow-complex tachycardia suggests atrial fibrillation or flutter with variable block

Regular wide-complex tachycardia should be treated as VT until proven otherwise

Irregular wide-complex tachycardia suggests AF with aberrancy or pre-excited AF (WPW)

AV dissociation or capture/fusion beats in a wide-complex tachycardia favor ventricular tachycardia

P Waves

P waves represent atrial electrical activity arising from the sino-atrial (SA) node

Sinus rhythm has one P wave before every QRS with a constant PR interval

Sinus P waves are upright in leads I and II and inverted in aVR

Absent P waves - think AF (Atrial Fibrillation) (most common), sinoatrial blocks, junctional rhythms, or ventricular rhythms

A bifid P wave suggests left atrial enlargement

A peaked P wave (P-pulmonale) suggests right atrial hypertrophy; hypokalaemia can mimic this pattern

Atrial flutter produces sawtooth flutter waves best seen in leads II, III, and aVF

Typical atrial flutter rate is about 300 bpm

PR Interval

Normal PR interval is 0.12 to 0.2 seconds, measured from start of P wave to start of QRS complex

1st degree heart block: PR interval greater than 0.2 seconds

Wolf-Parkinson-White syndrome (WPW): PR interval less than 0.12 seconds with a delta wave (slurred upstroke on R wave)

Wenckebach phenomenon (Mobitz Type I): Progressively prolonging PR interval until a QRS is dropped, then the cycle repeats

Mobitz Type II: Constant PR interval with intermittently dropped QRS complexes

3rd degree (Complete) heart block: P waves present but no association with QRS complexes (atria and ventricles beat independently)

PR depression in all leads with PR elevation in aVR suggests pericarditis

QRS Complexes

Normal QRS duration is less than 0.12 seconds (or 3 small boxes)

QRS prolongation may indicate sodium channel blockade or bundle branch block (BBB)

MARROW and WILLIAM for Bundle Branch Block

MARROW = Right bundle branch block → M shaped (RSR') pattern in V1, W shaped pattern in V6

WILLIAM = Left bundle branch block → W shaped (QS) pattern in V1, M shaped pattern in V6

In RBBB, lead V1 shows an M-shaped (RSR') pattern — think "M" from M-ARROW. The delayed right ventricular depolarisation creates a second R wave (R prime).

In RBBB, lead V6 shows a W-shaped pattern with a broad terminal S wave (reciprocal of the V1 RSR').

In LBBB, lead V1 shows a W-shaped (QS) pattern — think "W" from W-ILLIAM. The septum depolarises right-to-left (opposite normal), creating a deep QS complex.

In LBBB, lead V6 shows an M-shaped pattern with a broad notched R wave (delayed left ventricular activation).

Left bundle branch block (example ECG)Wikimedia Commons
Right bundle branch block (example ECG)Wikimedia Commons

R Wave Progression

Normal R wave transition occurs around V3 to V4

Poor R wave progression can suggest anterior MI (or lead misplacement)

Q Waves

A pathological Q wave is defined as: width more than 40ms (1mm), OR depth more than 25% of R wave, OR depth more than 2mm

ST Segments

ST elevation/depression is measured from the J point (junction of QRS and ST segment)

Significant ST elevation: In chest leads ≥2mm in 2+ leads; In limb leads ≥1mm

Horizontal or downsloping ST depression in contiguous leads suggests subendocardial ischemia

QT Interval

QT prolongation can lead to Torsades de Pointes (polymorphic VT), causing syncope or sudden death

Quick screen: the QT interval should be less than half the preceding R-R interval (rough check when HR is 60-100)

QTc (Bazett formula) = QT / √RR where QT and RR are measured in seconds

Corrects QT interval for heart rate to identify true QT prolongation.

QTc longer than 500 ms markedly increases torsades risk

Calcium effects on QT interval: Hypocalcaemia [] QT; hypercalcaemia [] QT

Treatment for Torsades de Pointes includes Magnesium, Potassium infusion, and/or overdrive pacing

Long QT on ECGWikimedia Commons

T Waves

Peaked T waves (tall, narrow, symmetric) are the earliest ECG sign of hyperkalaemia — check K+ urgently. Also consider hyperacute STEMI (asymmetric, broad-based T waves in a territorial distribution).

Severe hyperkalaemia on ECG

The most common pathological cause of T wave inversion is myocardial ischaemia.

Clinical pearl: Always consider ACS (Acute Coronary Syndrome) when you see new T wave inversions.

T wave inversion in V1-V4 with right axis deviation suggests pulmonary embolism (RV (Right Ventricle) strain pattern)

Deep T wave inversions in the context of neurological symptoms suggest major stroke (cerebral T waves)

Other Waves

U waves (extra wave after T wave) suggest hypokalaemia

J waves (Osborn waves) suggest hypothermia

Epsilon waves (small terminal deflection in V1-V3) indicate Arrhythmogenic right ventricular cardiomyopathy (ARVC)

ECG MCQs (image-first)

SBAeasyECGrate calculationbasics
Using the rhythm strip (25 mm/s), estimate the heart rate.
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SBAeasyECGsinus rhythmbasics
Look at the rhythm strip (lead II). What rhythm is shown?
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SBAmediumECGST elevationSTEMIbasics
Look at the anterior lead view (V1–V4). Which statement best describes the ST (ST Segment) segment?
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SBAmediumECGaxis
Look at the limb-lead ECG (Electrocardiogram). Lead I is predominantly positive, aVF is predominantly negative, and lead II is also negative. What is the cardiac axis?
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SBAeasyECGatrial fibrillationarrhythmia
Look at the rhythm strip (lead II). What rhythm is shown?
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SBAmediumECGatrial flutterarrhythmia
Look at the rhythm strip. The baseline shows sawtooth flutter waves with a regular ventricular response. What is the rhythm?
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SBAmediumECGSVTarrhythmia
Look at the rhythm strip. There is a regular narrow-complex tachycardia at ~180 bpm with no clearly visible P waves. What is the most likely rhythm?
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SBAhardECGWPWarrhythmia
Look at the rhythm strip in a patient with known WPW. What is the most likely rhythm?
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SBAmediumECGheart block
Look at the rhythm strip. The PR (Per Rectum) interval is 280 ms and constant across beats. What is the most likely diagnosis?
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SBAmediumECGbundle branch block
Look at the precordial leads (V1–V6). V1 shows an RSR' (M-shaped) complex and V6 shows a broad terminal S wave with QRS (QRS Complex) 140 ms. What is the diagnosis?
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SBAmediumECGWPWpre-excitation
Look at the rhythm strip. There is a short PR (Per Rectum) interval (<0.12 s) with a slurred upstroke at the start of the QRS (QRS Complex) (delta wave). What syndrome does this represent?
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SBAmediumECGlong QTintervals
Look at lead II. The QT (QT Interval) interval occupies more than half of the RR (Respiratory Rate) interval. Which abnormality is present?
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SBAmediumECGSTEMIinferior MI
Look at the inferior lead view (II, III, aVF). What territory shows ST (ST Segment) elevation?
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SBAeasyECGhyperkalaemiaelectrolytes
Look at the ECG (Electrocardiogram) image showing tall, peaked T waves with a 'tented' appearance. Which electrolyte abnormality should you suspect first?
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SBAhardECGTorsadesarrhythmia
Look at the rhythm strip: polymorphic VT (Ventricular Tachycardia) twisting around the baseline. Which treatment should be given immediately?
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SBAmediumECGpericarditischest pain
Look at the ECG (Electrocardiogram). There is PR (Per Rectum) segment depression in most leads with PR (Per Rectum) segment elevation in aVR and pleuritic chest pain. What is the likely diagnosis?
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Rhythm Strip Recognition

SBAmediumrhythm recognitionVFcardiac arrest
A patient is found unresponsive. The following rhythm strip is displayed on the monitor. What is the rhythm and is it shockable?
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SBAmediumrhythm recognitionVTwide complex tachycardia
Syncope

What is this rhythm?

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SBAmediumrhythm recognitionatrial flutterAF
HR
75bpm

What is the most likely diagnosis?

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8. IV Cannulation

  1. Consent and explain procedure
  2. Hand hygiene and apply non-sterile gloves
  3. Apply tourniquet 10-15cm above insertion site
  4. Select vein and clean site (2% chlorhexidine, allow to dry)
  5. Insert cannula at 10-30° angle, bevel up
  6. Advance until flashback seen in chamber
  7. Lower angle and advance slightly, then slide cannula off needle
  8. Release tourniquet, apply pressure proximally, remove needle
  9. Secure with transparent dressing
  10. Flush with 5-10mL saline to confirm patency

9. Toxicology

Clinical Approach: RRSI DEAD

RRSI DEAD - Toxicology Management
  • R - Resuscitation (ABCDE, use Ringer's Lactate over NS to avoid worsening acidosis)
  • R - Risk assessment (predict clinical course: benign vs severe)
  • S - Supportive care (FAST HUGS IN BED Please)
  • I - Investigations/monitoring
  • D - Decontamination (activated charcoal, whole bowel irrigation)
  • E - Enhanced elimination (dialysis, urinary alkalinisation, multi-dose charcoal)
  • A - Antidote (if available)
  • D - Disposition (ward, ICU, psych review)

Supportive Care: FAST HUGS IN BED Please

FAST HUGS IN BED Please - ICU Supportive Care
  • F - Fluids and Feeding
  • A - Analgesia, Antiemetics
  • S - Sedation, Spontaneous breathing trial
  • T - Thromboprophylaxis, Tetanus
  • H - Head up 30° (if intubated)
  • U - Ulcer prophylaxis
  • G - Glucose control
  • S - Skin/eye care, Suctioning
  • I - Indwelling catheter
  • N - Nasogastric tube
  • B - Bowel care
  • E - Environment (temperature, delirium prevention)
  • D - De-escalation (end of life, stop unnecessary treatments)
  • P - Psychosocial support

Common Toxidromes

ToxidromeCausesKey FeaturesTreatment
OpioidHeroin, fentanyl, morphineMiosis, respiratory depression, ↓LOCNaloxone (titrate to RR)
SedativeBenzos, barbiturates, GHBSedation, respiratory depressionSupportive (flumazenil rarely)
SympathomimeticAmphetamines, cocaine, MDMAMydriasis, tachycardia, HTN, hyperthermiaBenzos, cooling
AnticholinergicTCAs, antihistamines, atropine"Mad, bad, red, dry" - confusion, tachycardia, mydriasis, dry skinSupportive + benzos; consider physostigmine only in selected cases with toxicology advice (Poisons 13 11 26)
CholinergicOrganophosphates, nerve agentsDUMBELLS: diarrhea, urination, miosis, bradycardia, emesis, lacrimation, salivationAtropine + pralidoxime
SerotonergicSSRIs + MAOIs, tramadolClonus (LL > UL), hyperreflexia, hyperthermiaCyproheptadine, benzos, cooling
Warning

Physostigmine in anticholinergic toxicity is NOT routine

Contraindications:

  • TCA toxicity suspected (QRS (QRS Complex) widening)
  • Mixed or unknown overdose

Only consider for severe pure anticholinergic delirium with senior/toxicologist advice (Poisons Info 13 11 26).

Opioid triad: Miosis + Respiratory depression + Decreased LOC

Clinical Pearl

Anticholinergic mnemonic: "Mad as a hatter, blind as a bat, dry as a bone, red as a beet, hot as a hare"

Decontamination

MethodIndicationContraindication
Activated charcoal (50g)Within 2h of IR ingestion, 4h of SRAcids/alkalis, metals (Fe, Li), alcohols, hydrocarbons
Whole bowel irrigationMassive OD, metals, sustained-releaseBowel obstruction, perforation

Enhanced Elimination

PLASMA TV - Dialysable Toxins
  • P - Phenobarbitol
  • L - Lithium
  • A - Acidosis (severe)
  • S - Salicylates
  • M - Metformin
  • A - Alcohols (toxic: methanol, ethylene glycol)
  • T - Theophylline
  • V - Valproic acid

Key Antidotes

ToxinAntidote
ParacetamolNAC (N-Acetylcysteine)
OpioidsNaloxone
BenzodiazepinesFlumazenil (use cautiously)
Beta-blockersHigh-dose insulin euglycaemic therapy (HIET)
Calcium channel blockersHIET, IV Calcium
DigoxinDigibind (Fab fragments)
TCAsSodium bicarbonate (for QRS widening)
WarfarinVitamin K, FFP/PCC
Methanol/ethylene glycolFomepizole or ethanol
OrganophosphatesAtropine + pralidoxime
SBAmediumtoxicologydecontamination
1y
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SBAeasytoxicologytoxidromes
M
HR
tachycardia
GCS
confused
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SBAmediumtoxicologydialysis
Which toxin on this list is classically dialyzable: digoxin, tricyclic antidepressants, lithium, benzodiazepines, paracetamol?
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10. Australasian Triage Scale (ATS)

CategoryMaximum WaitDescriptionExample
ATS 1ImmediateLife-threateningCardiac arrest, airway obstruction
ATS 210 minutesImminent life-threateningChest pain, severe dyspnoea, major trauma
ATS 330 minutesPotentially life-threateningModerate dyspnoea, persistent vomiting
ATS 460 minutesPotentially seriousMinor trauma, urinary symptoms
ATS 5120 minutesLess urgentReview of results, minor complaints

Performance thresholds: ATS 1 = 100%, ATS 2 = 80%, ATS 3 = 75%, ATS 4 = 70%, ATS 5 = 70%

SBAeasytriageATS
A patient arrives in cardiac arrest with no pulse. What is the maximum wait time under the ATS?
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SBAeasytriageATS
Chest pain

What is the ATS maximum wait time?

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SBAeasytriageATS
A stable patient has moderate dyspnoea but no red flags. What is the ATS maximum wait time?
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SBAeasytriageATS
A patient presents with a minor laceration and stable observations. What is the ATS maximum wait time?
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SBAeasytriageATS
A patient attends for review of stable results with no acute symptoms. What is the ATS maximum wait time?
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Three Phases of ED Management

PhaseTimeframeFocus
Resuscitation0-10 minutesABCDE, life-saving interventions
Secondary care10-60 minutesHistory (AMPLE), examination, specific treatment
Tertiary care1-24 hoursConsult, Continuity, Communicate (3 C's)

11. Post-Resuscitation Care

Chain of Survival

4 Links in the Chain of Survival
  1. Early recognition and call for help
  2. CPR (do it early; buys time)
  3. Defibrillation (do it early; definitive for VF/pVT)
  4. Post-resuscitation care (optimise outcomes)

Definitive treatment for VF/pVT is early defibrillation.

ROSC - What Next?

Evidence of ROSC:

  • Sudden increase in end-tidal CO2 (>40 mmHg)
  • Arterial waveform on monitor
  • Purposeful movement
  • Spontaneous breathing

Post-ROSC Care Priorities

DomainTargetAction
AirwaySecureConsider intubation if GCS (Glasgow Coma Scale) less than 8
BreathingSpO2 (Peripheral Oxygen Saturation) 94-98%, normocapniaAvoid hyperoxia (↑ free radicals) and hypocapnia (↓ cerebral perfusion)
CirculationMAP (Mean Arterial Pressure) >65, SBP (Systolic Blood Pressure) >100Fluids, vasopressors as needed
DisabilityNormoglycaemiaTreat seizures, avoid hyperthermia
Investigations12-lead ECG (Electrocardiogram), CXR (Chest X-Ray)Identify cause (STEMI (ST-Elevation Myocardial Infarction) → cath lab)
TemperatureTemperature controlActively prevent fever (≤37.5°C) for at least 72h in comatose survivors
SBAmediumpost-resuscitationoxygen therapy
A patient achieves ROSC (Return of Spontaneous Circulation) after 15 minutes of CPR (Cardiopulmonary Resuscitation). They remain unconscious. What is the target SpO2 (Peripheral Oxygen Saturation) range?
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12. Airway Management — Difficult Airway

LEMON Assessment for Difficult Intubation

LEMON — Predict Difficult Intubation
  • Look externally — facial trauma, large tongue, short neck, obesity, beard
  • Evaluate 3-3-2 — 3 fingers mouth opening, 3 fingers hyomental distance, 2 fingers thyromental distance
  • Mallampati score — Class I–IV; III–IV predict difficult laryngoscopic view
  • Obstruction — epiglottitis, abscess, tumour, foreign body
  • Neck mobility — C-spine collar, ankylosing spondylitis, rheumatoid arthritis

LEMON is a bedside assessment to predict difficult direct laryngoscopy. Multiple positive features → prepare backup airway plans.

Rapid Sequence Intubation (RSI (Rapid Sequence Intubation))

RSI (Rapid Sequence Intubation) = simultaneous induction agent + neuromuscular blocker after pre-oxygenation, without bag-mask ventilation (to avoid gastric insufflation and aspiration).

StepActionKey Detail
1. PreparationEquipment, drugs, team rolesCheck laryngoscope, ETT (+ 1 size up/down), bougie, suction, backup LMA (Laryngeal Mask Airway)
2. Pre-oxygenation3 min tidal breathing on NRB or HFNCCreates O₂ reserve (~8 min apnoea time in healthy adults)
3. Pre-treatmentConsider fentanyl (blunt sympathetic response)Optional — for raised ICP (Intracranial Pressure) or cardiovascular disease
4. Paralysis + InductionInduction agent → NMBA immediately afterKetamine 1–2 mg/kg + rocuronium 1.2 mg/kg (or suxamethonium 1.5 mg/kg)
5. PositioningSniffing position (ear to sternal notch alignment)Ramped position for obese patients
6. PlacementLaryngoscopy → pass ETT through cordsConfirm with ETCO₂ waveform (gold standard)
7. Post-intubationSecure tube, CXR, ventilator settingsSedation + analgesia infusion
Warning

Confirm ETT placement with continuous end-tidal CO₂ waveform — auscultation alone is NOT reliable. No waveform = not in trachea until proven otherwise.

Can't Intubate, Can't Oxygenate (CICO (Can't Intubate, Can't Oxygenate))

Warning

CICO (Can't Intubate, Can't Oxygenate) is a life-threatening emergency. If you cannot intubate AND cannot oxygenate with BVM or supraglottic device → immediate front-of-neck access (FONA).

The Vortex Approach

The Vortex is a cognitive aid for airway management:

Three upper airway lifelines (max 3 attempts each):

  1. Face mask ventilation (BVM)
  2. Supraglottic airway (LMA (Laryngeal Mask Airway))
  3. Endotracheal tube (ETT via laryngoscopy)

If all three lifelines fail → you are in the green zone (CICO)immediate FONA.

Front-of-Neck Access (FONA)

TechniqueMethodKey Points
Scalpel cricothyroidotomyStab incision through cricothyroid membrane → bougie → tubePreferred technique in adults; fastest and most reliable
Needle cricothyroidotomy14G cannula through cricothyroid membrane → jet ventilationTemporising only; limited ventilation; risk of barotrauma
Surgical tracheostomyFormal incision below cricoidDefinitive but slow; not for emergencies
Clinical Pearl

Landmark: Palpate the thyroid cartilage → slide down to the cricothyroid membrane (soft depression between thyroid and cricoid cartilage). This is your FONA target.

SBAmediumCICOairwayVortexFONA
During an emergency intubation, three attempts at direct laryngoscopy fail and SpO₂ is dropping. BVM ventilation is ineffective and an LMA (Laryngeal Mask Airway) cannot be placed. What is the next step?
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13. Altered Mental State

Structured Approach: AEIOU-TIPS

AEIOU-TIPS — Causes of Altered Mental State
  • Alcohol — intoxication, withdrawal
  • Epilepsy / Endocrine — post-ictal, status epilepticus, hypoglycaemia, thyroid storm, Addisonian crisis
  • Insulin — hypoglycaemia, DKA, HHS
  • Opiates / Overdose — drug toxicity, poisoning
  • Uraemia — renal failure, hepatic encephalopathy
  • Trauma — head injury, raised ICP
  • Infection — meningitis, encephalitis, sepsis
  • Psychiatric — catatonia, conversion disorder (diagnosis of exclusion)
  • Stroke / SAH — ischaemic, haemorrhagic, subarachnoid

Immediate priorities in altered mental state:

  1. ABCDE — secure airway if GCS less than 8
  2. Check BSL — treat hypoglycaemia immediately (50 mL of 50% dextrose IV)
  3. Check pupils — asymmetry suggests structural cause (herniation, stroke)
  4. Consider naloxone — if pinpoint pupils + respiratory depression
Warning

Always check BSL in altered mental state — hypoglycaemia is the most rapidly reversible and dangerous cause to miss.

InvestigationLooking For
BSL (bedside)Hypoglycaemia (less than 4 mmol/L)
ABG/VBGMetabolic acidosis (DKA, toxic ingestion), hypercapnia
FBC, UEC, LFTs, CRPInfection, renal/hepatic failure, electrolyte disturbance
Blood culturesSepsis
CT brainStroke, haemorrhage, raised ICP, mass lesion
Lumbar punctureMeningitis, encephalitis, SAH (if CT negative)
Toxicology screenDrug overdose, poisoning
ECGArrhythmia, drug toxicity (QTc prolongation)
Clinical Pearl

Time-critical causes to exclude first: Hypoglycaemia → Meningitis → Stroke. All three have interventions that are time-dependent.

See also: Headache Differentials, Status Epilepticus (Week 7 — Disability)

SBAmediumaltered-mental-stateopioidnaloxone
45y
RR
6/min↓↓
GCS
6↓↓

What is the most important immediate intervention?

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Week 1 Study Checklist

Click to expand or view deep dives

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DRSABCD algorithm
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COACHED defibrillation sequence
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Shockable vs non-shockable rhythms
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4 H's and 4 T's with treatments
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A PINCH high-risk medications
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Drug timing in ALS
--
Induction agent selection
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Suxamethonium contraindications
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PK changes in critical illness
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Common toxidromes
--
PLASMA TV dialysable toxins
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Key antidotes
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Australasian Triage Scale
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Post-ROSC care
--
LEMON difficult airway assessment
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RSI sequence
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CICO and Vortex approach
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AEIOU-TIPS for altered mental state